Equine Med - Skele MM Disorders 2

pbhati17's version from 2018-03-18 02:00


Question Answer
what are the main reasons you'd see a non-exertional myopathy?Traumatic (injury/anesthesia), genetic/hereditary, infectious (immune mediated), nutritional, toxic
classic signs of a HYPP attack?Sweating, weak, diffuse muscle fasciculations. Flaring nostrils, facial mm spasm...having trouble breathing...head twitching... dull mentation (out of it). 3rd eyelid prolapse, inc RR. Generally NOT painful, and no inflammation. Most recover uneventfully but rarely there can be acute death if resp or CV affected enough
what does HYPP stand for?Hyperkalemic periodic paralysis
WHO gets HYPP?Genetic disease (AUTOSOMAL DOMINANT) of Quarter Horses (they are halter horses- want them to look like body builders)
Which ion channel is affected with HYPP?Na+--- NOT K+ (in the muscle membrane not nerves)
explain the pathogenesis of HYPPMutation in voltage-gated Na channels (Na!! NOT K!!!!) In normal situation, mm gets signal, Na channel opens, Na goes from out to in, channel closes. In these HYPP horses, once the gate is doesn't close again--> CONSTANT DEPOL (hence fasciculations and such). Even slight changes in the extracellular K+ level (fluctuations) can cause opening of these channels which get stuck open. These hyperexcitable muscles lead to paralysis. (death usually bc respiratory arrest)
what will K+ plasma levels and CK be like with HYPP?K+ might be elevated or WNL. CK WILL BE NORMAL because it isn't muscle damage, it's just constant mm stimulation.
how can you definitively diagnose HYPP? what can results look like?Genetic test- look for SCN4A gene with blood or hair samples. It is an autosomal dominant trait, so results can be NN (normal i assume?) NH, or HH
based on the genetic test, who is most likely to have the worst problems with HYPP?heterozygous positive less likely to have a severe attack than homozygous positive
how do you tx hypp-- what is the main goal?Main goal is to dec K+ levels in plasma (bc K+ levels are what trigger the Na++ channels to open up and then they stick open) so if there is a MILD attack: Karo syrup (NOT MOLASSES-- THAT IS SUPER HIGH IN K+), grain. If there is a SEVERE attack: IV Bicarb, IV dextrose, Calcium gluconate, insulin
why are we giving sugar and insulin with HYPP severe attacks?because sugar+insulin--> K+ gets pushed into cells with it (lower plasma K--> stop triggering channels to open)
why give calcium gluconate to a HYPP attack horse?cardioprotective infusion. dont actually maintain K but protects mm and makes them more apt to fxn normally.
**What foods are high in K+ that you should avoid in HYPP? NO alfalfa, bran, molasses based feeds
what do you want HYPP horse's diet to look like?Diet low in potassium!!! AVOID alfalfa, bran, molasses based feeds, and also avoid rapid feed changes bc even just variations in K+ level of hay can set them off. Provide regular exercise,
What drug can you give to help manage HYPP- how does it work?Acetazolamide! This is a diuretic-- a carbonic anhydride inhibitor. It causes horses to retain bicarb and they will be slightly alkalotic, which encourages K+ to go into cells in exchange for H+ to go out. ALSO it inc K+ excretion in urine, AND stimulate insulin secretion.
what should you know about breeding HYPP horses?H/H foals no longer registered with AQHA-- prolly shouldn't breed them.
mitochondrial myopathy- who gets this? What is kinda the deal?ARABIANS- it's basically a malig hyperthermia thing- esp under anesthesia.
aside from PSSM and HYPP... what OTHER genetic condition can QHs get? (yikes)Glycogen branching enzyme deficiency
who gets Glycogen branching enzyme deficiency, whats the deal with it?QHs, kinda like PSSM, but more severe signs and early on- not really related to exercise. not very common.
are CN signs usually uni or bilateral?usually unilateral.


Question Answer
WMD aka?Nutritional Myodegeneration, Nutritional muscular dystrophy
what is WMD? what is the pathogenesis?It is a A non-inflammatory degenerative disease of skeletal and/or cardiac muscle. It is caused by a deficiency in Vit E/ selenium (most commonly a prob is pacific NW or western Canada.) Usually selenium is more to blame. Vit E/selenium are VITAL free radical scavengers (important antioxidants) which prevent free radical and calcium damage to cell membranes. Selenium is an important component of glutathione peroxidase
what are the 3 clinical syndromes of WMD?(1) cardiac (2) subacute skeletal form (3) chronic myopathy form
who usually gets the cardiac form of WMD? how does it present?Usually FOALS AND WEANLINGS get this, you see ACUTE ONSET of cardiac decompensation--> pulm edema, dyspnea, heart murmurs. Death within 24hrs or found dead
who usually gets the subacute skeletal mm form of WMD? how does it present?once again, usually foals and weanlings, present with Profound weakness, stiff, spastic gait. They have tense and painful muscles, ****DYSPAGIA (masseter mm seem to take the brunt of it~ and poor suckle reflex. They can be BAR or depressed.
who usually gets the chronic myopathy form of WMD? how does it present?this is in ADULT horses, you see ***Masseter atrophy and degeneration, Dysphagia, inability to eat, weight loss, limited range of jaw motion, and occasional tongue involvement.
what will chem/UA look like with WMD?inc CK and AST, +/- myoglobinuria.
what is the most accurate thing you can measure to dx WMD?measuring glutathione peroxidase levels is more accurate than measuring selenium (one sample is not 100% accurate)....obv you can also do a mm bx
how do you tx WMD?NONE avail for CARDIAC form. :(. for subacute and chronic forms: E/Se injections (1ml/100lbs IM)-- although these shots HAVE been linked to severe reactions. Can also consider oral supplementation. Also rest and supportive care: feeding, NSAIDs, fluids, etc
prevention of NMD is particularly important in who?(nutritional myodegeneration= WMD) esp important in PREG MARES.
What are Monensin, Salinomycin, Lasalocid?IONOPHORES
who ARE ionophores for? who are they not for?FOR chickens and cows, NOT FOR HORSES! SUPER SENSITIVE!
What happens if a horse ingests ionophores?only 2-3mg/kg can be toxic. massive heart failure. go into cells, jack with golgi apparatus. not sure why picks cardiac mm in horses-- but goes in and causes cardiac degeneration. see acute, severe heart failure. There is no tox screen- cant sample of blood and look at ionophore exposure. Hx and necropsy
how do you dx ionophore tox?CAN'T DETECT IN BLOOD/BODY! can only dx with hx or necropsy
tx ionophore tox?only supportive care/activated charcoal
injection site severe infections often infected with...clostridium. Clostridium myonecrosis.
What should you know about banamine???DO NOT GIVE IM. causes severe necrosis. Give IV or squirt in mouth.
Clostridium necrosis is usually caused by which species?Typically C. perfringens Type A (CPA-- neigh neigh). Also C. septicum and C. sporogenes
clostridium myonecrosis usually happens from..most commonly due to injections. Could be juncture wounds/ insect bites/ etc tho
how does clostridium myonecrosis present?Rapid onset of severe local swelling, heat, pain and crepitus (=GAS PRODUCTION)...lead to Depressed, high fever, tachycardia--> SEVERE TOXEMIA, SHOCK, AND DEATH
how can you tell the diff between Injection site reaction/abscess and clostridial myonecrosis?injection site reaction/abscess should have a NORMAL CBC. With clostridial myonecrosis they feel sick and crappy, their CBC is not normal, and you can probably feel crepitus (will turn black in palominos and white horses)
if you take an aspirate of clostridium myonecrosis and look at it under the microscope, what will it look like?G+ rods, need anaerobic culture
how do you treat clostridial myonecrosis?EARLY and AGGRESSIVE!! Penicillin double dose every 4-6 hours (it's G positive!! and once again, DOC for clostridium). If you want broad coverage, can consider adding in G- coverage and metronidazole. Also provide supportive care (fluids, NSAIDs,) might consider Surgical debridement & fasciotomy. Can try antitoxin (only for CP C and D tho). Prog guarded (bc of systemic effects from toxins and sequelae (IMHA, DIC, laminitis, colitis bc on abx... ) )

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